BackgroundOxidized phosphatidylcholines (oxPC) and lysophosphatidylcholine (lysoPC) generated during the formation of oxidized low-density lipoprotein (oxLDL) are involved in atherosclerotic lesion development. We investigated the time course-changes in phosphatidylcholine (PC) molecular species during oxidation of LDL to determine how those atherogenic PCs are produced.MethodsHuman and rabbit LDLs were pretreated with or without a selective platelet-activating factor acetylhydrolase (PAF-AH) inhibitor. LDL was oxidized by incubation with copper sulfate, and PC profiles were analyzed by liquid chromatography-tandem mass spectrometry.ResultsWhen human LDL was oxidized, the peak areas for polyunsaturated fatty acid (PUFA)-containing PC species dramatically decreased after a short lag period, concomitantly lysoPC species increased sharply. Although a variety of oxPC species containing oxidized fatty acyl groups or cleaved acyl chains are formed during LDL oxidation, only a few oxPC products accumulated in oxLDL: 1-palmitoyl-2-(9-oxo-nonanoyl) PC and long-chain oxPC with two double bonds. Pretreatment of LDL with the PAF-AH inhibitor greatly reduced lysoPC production while it had no effect on lipid peroxidation reactions and oxPC profiles. Rabbit LDL, which has a different composition of PC molecular species and needs a longer time to reach achieve full oxidation than human LDL, also accumulated lysoPC during oxidation. The increase in lysoPC in rabbit oxLDL was suppressed by pretreatment with the PAF-AH inhibitor. The major oxPC species formed in rabbit oxLDL were almost the same as human oxLDL.ConclusionsThese results suggest that lysoPC species are the major products and PAF-AH activity is crucial for lysoPC generation during oxidation of LDL. The oxPC species accumulated are limited when LDL is oxidized with copper ion in vitro.

The hybrid hydrogel composed of tubular aluminosilicate nanofiber, “imogolite,” and pepsin was prepared in a simple manner. We confirmed the formation of a network structure of imogolite in hydrogel by FE-SEM observations. Pepsin immobilized onto imogolite showed enzymatic activity after repeated reactions.

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Summary Background: The origin of moisture in diarrhea feces is unknown but may represent the unabsorbed part of intestinal contents or alternatively, body fluid excreted into the digestive canal. If the latter mechanism contributes to moisture in the feces, active transport of water (H 2 O) associated with ion exchange channels may be involved. Objective: To investigate this possibility we measured the content of moisture and minerals (sodium [Na] [Mn]) in feces collected during a 12-d metabolic study on 11 young Japanese female students. Design: The study was carried out as part of a human mineral balance study. The same quantity of food was supplied to each of the subjects throughout the study without consideration of body weight. Fecal specimens were collected throughout the study and were separated into those originating from the diet during the balance period based on the appearance of the ingested colored marker in the feces. Results: The moisture content of the feces ranged between 53 and 92%. Na content in the feces was low and stable when the moisture content was below 80%, whereas it increased up to serum levels when the moisture content increased above 80%. On the other hand, K content increased when compared to dry matter base. However, when comparing concentration/g moisture, K content increased when moisture was below 70%, but decreased when this rose above 70%.

Tetranuclear and hexanuclear nickel(II) complexes with N,N′-bis(2-hydroxy-3,5-dimethylbenzyl)-N,N′-dimethyl-1,2-ethanediamine (H2L), [Ni4L2(CH3COO)4]·4THF and [Ni6L3(OH)4(NO3)2(H2O)2]·2DMF, have been synthesized and characterized by X-ray crystallography, electronic spectroscopy and magnetic susceptibility measurement.